Elucidate that fatigue-induced viral factors affect the onset of depression
| Project/Area Number |
16H07220
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Psychiatric science
|
|---|
| Research Institution | Jikei University School of Medicine |
|---|
Principal Investigator |
Oka Naomi 東京慈恵会医科大学, 医学部, 助教 (00704503)
|
|---|
| Project Period (FY) |
2016-08-26 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| Keywords | うつ病 / ウイルス / ストレス / 精神疾患 / 抗うつ薬 / ウイルス学 / ストレス脆弱性 |
|---|
| Outline of Final Research Achievements |
Small protein encoded by the intermediate stage transcript of HHV-6 (SITH-1) is a latent infected protein expressed by the human herpes virus (HHV-) 6 reactivated in a fatigue or stress-dependent manner. In order to elucidate the mechanism by which SITH-1 is involved in the development of depression, we created a SITH-1 expressing mouse model (SITH-1 mouse). SITH-1 mice showed depression-like behavior and stress vulnerability.
Further studies showed that SITH-1 expression increased intracellular calcium concentration and subsequently induced apoptosis in the olfactory bulb, resulting in inhibition of hippocampal neurogenesis. Therefore, it is considered that SITH-1 mouse had a property of impaired stress response.
|
Report
(3 results)
Research Products
(4 results)
